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Table of Contents
Vol. 55, No. 1, 2003
Issue release date: August 2003
Section title: Original Paper
Hum Hered 2003;55:46–50
(DOI:10.1159/000071809)

Pleiotropy and Heterogeneity in the Expression of Atherogenic Lipoproteins: The IRAS Family Study

Hokanson J.E.a · Langefeld C.D.b · Mitchell B.D.c · Lange L.A.b · Goff Jr. D.C.b · Haffner S.M.d · Saad M.F.e · Rotter J.I.e,f
aDepartment of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, Colo., bWake Forest University School of Medicine, Winston-Salem, N.C., cUniversity of Maryland, Baltimore, Md., dUniversity of Texas Health Sciences Center at San Antonio, San Antonio, Tex., eUniversity of California at Los Angeles, fCedars-Sinai Medical Center, Los Angeles, Calif., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 10, 2003
Accepted: April 16, 2003
Published online: August 06, 2003
Issue release date: August 2003

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 3

ISSN: 0001-5652 (Print)
eISSN: 1423-0062 (Online)

For additional information: http://www.karger.com/HHE

Abstract

Objective: Dyslipidemia is an important determinant of coronary disease. Phenotypic correlations between atherogenic lipids are well established, but the contribution of common genetic influences is less clear. Methods: This study investigates the pair-wise genetic (ρg) and environmental (ρe) correlations between apoB, LDL-C, HDL-C, and triglyceride (Tg) from Hispanic and African American families of the IRAS Family Study. Results: Heritability estimates (hcirc;2) indicate significant genetic effects on apoB (hcirc;2 = 0.46 ± 0.05), LDL-C (hcirc;2 = 0.40 ± 0.05), HDL-C (hcirc;2 = 0.47 ± 0.05), and Tg (hcirc;2 = 0.35 ± 0.05) (all p < 0.001). Genetic and environmental correlations were strong for apoB – LDL-C (ρg = 0.87, ρe = 0.84), apoB – Tg (ρg = 0.38, ρe = 0.65), and HDL-C – Tg (ρg = –0.42, ρe = –0.46). Environmental correlations were strong for apoB – HDL-C (ρe = –0.40), LDL-C – HDL-C (ρe = –0.24), and Tg – LDL-C (ρe = 0.33) with weak genetic correlations for these pairs (ρg = –0.09, 0.10, 0.09 respectively). Conclusions: These results suggest multiple pathways leading to atherogenic dyslipidemia. There are common genetic and environmental influences contributing to variations in apoB and LDL-C as well as apoB and Tg. In addition, the inverse relation between Tg and HDL-C appears to have both genetic and environmental basis. Identifying genes involved in atherogenic dyslipidemia will require careful dissection of the genetic architecture of these pathways.

© 2003 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 10, 2003
Accepted: April 16, 2003
Published online: August 06, 2003
Issue release date: August 2003

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 3

ISSN: 0001-5652 (Print)
eISSN: 1423-0062 (Online)

For additional information: http://www.karger.com/HHE


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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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